Biological Psychiatry

Original Paper
Neuropsychobiology 1994:30:7-10

Department of Neuropsychiatry,
Kanazawa University School o f Medicine,
Kanazawa, Japan

Case Study of
Monosymptomatic Delusion of
Unpleasant Body Odor with
Structural Frontal Abnormality

Key Words

Abstract

Delusion
Paranoid disorder
Monosymptomatic hypochondriacal
psychosis
Organic delusional syndrome

We report a 63-year-old man with a monosymptomatic delusion of unpleasant
body odor contracted at the age of 61 years, who believed that his body reeked
of some type of paint. He had symmetrical atrophy in the bilateral frontal
lobes of unknown etiology on MRI. Further, quantitative rCBF measurement
with SPECT brain scan using 99mTc-HMPAO showed relative hypoperfusion
localized in the bilateral frontal lobes. EEG, neurological and neuropsycholog­
ical tests were all normal, including the WAIS-R and Wechsler Memory Scale
tests. However, he showed poor results on the Wisconsin Card Sorting test,
presumably on account of frontal dysfunction, attaining only two categories
with frequent perseverative errors. Although it is undetermined whether the
illness in this case can be classified as organic delusional syndrome or para­
noid disorder according to DSM-III-R criteria, these results imply that delu­
sions are associated with frontal lobe abnormality.

The pathogenesis of delusion, which is a representative
psychotic symptom, is an important and still unresolved
problem in the field of neuropsychiatry. Recently, Benson
and Stuss [ 1] postulated an association between delusion
and prefrontal malfunction based on descriptions of a
number of organic delusion syndromes associated with
frontal damage on computed tomographic (CT) scans,
e.g., a case with Capgras syndrome. The present report
provides supportive data for this hypothesis from neuro­
imaging and neuropsychological examinations in a spe­
cific case with monosymptomatic delusion of unpleasant
body odor contracted in late life.

Case Report
The patient was a 63-year-old right-handed man with an intro­
verted and earnest personality. After completing an 8-year schooling
he served for many years as an artisan in a factory making household
Buddhist altars. He brought up 2 children, a son and a daughter, sin­
gle-handedly after he divorced at the age of 41 years. He had no occu­
pation after retiring from the factory at the age of 60 years. Since the
marriage of his daugthcr 10 years previously he had been living with
his 37-year-old unmarried son. There was no evidence of any signifi­
cant medical illness including psychosis in either his own or his fami­
ly history. Further, he had no history of drug addiction, and did not
consume either alcohol or cigarettes.

Itsuki Jibiki
Department of Neuropsychiatry
Kanazawa University School of Medicine
13-1 Takaramachi
Kanazawa. Ishikawa Prefecture. 920 (Japan)

© 1994 S. Karger AG, Basel
0302-282X/94/0301-0007
$5.00/0

Downloaded by:
Karolinska Institutet, University Library
130.237.122.245 - 1/12/2019 1:43:31 AM

Itsuki Jibiki
Yasutake Kagara
Susumu Kisliizawa
Kenzo Kurokawa
Toshinobu Fukushima
Hisakazu Furuta
Nariyoshi Yamaguchi

Fig. 1. MRI findings, a-c Ti intensity-weighted axial images indicating frontal atrophy, d Intermediate intensityweighted axial image showing periventricular high intensity lesion. e L intensity-weighted axial image with multiple
small lacunes (arrow marks). R. right; L, left.

8

In the first psychiatric examination, his facial expression, gestures
and behavior appeared natural. His understanding, contact and atti­
tude during the interview were also normal. His general mental state
showed neither intellectual nor memory deficits with both his orien­
tation and consciousness level normal. He revealed no symptoms
except for the above-mentioned delusions and feeling of physical dis­
order. Personality change, too, was unlikely to be present in view of
the history outlined by the son. Routine physical and neurological
tests showed no abnormalities nor did routine neuropsychological
tests reveal any signs of aphasia, apraxia or agnosia. For the diagnosis

Jibiki/Kagara/Kishizawa/Kurokawa/
Fukushima/Furuta/Yamaguchi

Delusion and Frontal Lobe

Downloaded by:
Karolinska Institutet, University Library
130.237.122.245 - 1/12/2019 1:43:31 AM

One day in October, 1991. at the age of 61 years, he perceived an
intense smell of a type of paint he applied on a pillar in his house to
suppress white ants. Subsequently, he developed a delusional belief
of so-called 'unpleasant body odor’ in which his body recked of this
paint which he could not get rid of. Further, at the same time he
developed a hypochondriacal delusion in which his tongue and the
mucous membrane in his nose and mouth were affected, because of
the smell, with a feeling of physical disorder. As he felt the smell most
strongly when he was in his home, he often left his home. On Decem­
ber 15, 1992, he visited our clinic with his son.

Discussion

It is clear from the MRI findings that the present case
had an atrophied structural or organic abnormality in the
bilateral frontal lobes. The SPECT findings support this.
Further, his poor results on the WCST imply a frontal
abnormality, because it is known that this test is closely
associated with dorsolateral prefrontal function [2], His

illness characterized by the delusion of unpleasant body
odor and related symptoms contracted late in life would
have been diagnosed as ‘monosymptomatic hypochon­
driacal psychosis' as proposed by Munro [3] or paranoid
disorder on DSM-III-R criteria, had it not been for the
MRI findings. However, the present frontal abnormality
suggests that his illness should be classified as organic
delusional syndrome by DSM-III-R criteria, which means
that the delusion resulted from the organic frontal abnor­
mality. Benson and Stuss [1] stated that the delusion of
unpleasant body odor is not uncommon in organic delu­
sions, although they illustrated no cases with this delu­
sion. Further, Miller and Lesser [4] described that neuroimaging was useful for the diagnosis or pathogenetic
understanding in late-life psychosis. However, in the
present case, the origin of the atrophied frontal lobes is
unknown, since his illness is not symptomatically compat­
ible with any of the established organic cerebral diseases,
including degenerative diseases such as Alzheimer’s dis­
ease, Pick’s disease and dementia of frontal lobe type
reported by Gustafson [51 and Neary et al. [61. It is most
probable that the present frontal atrophy resulted from
relatively severe aging changes consisting of cerebral de­
generative and arteriosclerotic changes. Further, in the
present case, it is unknown when the frontal abnormality
developed, in particular with regard to the onset of the
delusion. Moreover, there is no direct evidence for dem­
onstrating a causal relation between the delusion and
frontal abnormality, although the disability in mental set
shifting on the WCST may be related to the disturbance of
reality testing underlying the delusion [1], Therefore, a
definite diagnosis of organic delusional syndrome in the
present case may be difficult.
It has been reported that a number of schizophrenic
patients have organic cerebral anomalies on CT or MRI,
e.g., small or atrophied frontal and temporal lobes, and
dilated lateral ventricle [7-9], Although these findings
imply that organic anomalies may partly contribute to the
origin of schizophrenia, they do not mean that schizo­
phrenia is an organic mental disorder beause many
schizophrenics have no organic anomalies on CT or MRI.
One may argue that the existence of an organic frontal
abnormality in the present case is compatible with that of
such organic anomalies in schizophrenics, not necessarily
leading to the diagnosis of organic delusional syndrome
but suggesting that there may be a number of paranoid
disorders having organic cerebral anomalies. Further, it
has been opined that the organic anomalies on MRI in
schizophrenics may be due to cerebral developmental dis­
orders [8]. But, in the present case, the frontal abnormali­

9

Downloaded by:
Karolinska Institutet, University Library
130.237.122.245 - 1/12/2019 1:43:31 AM

of his illness, a number of further examinations were carried out in
his neuroleptic-naive condition in our outpatient clinic over the sub­
sequent 2 weeks, as described below.
As shown in figure 1, MRI revealed symmetrical atrophy local­
ized in the bilateral frontal lobes with obvious dilatation of the ante­
rior portion of the longitudinal cerebral fissure (fig. la-c). Further,
slight periventricular cerebral arteriosclerotic change (fig. Id) and
multiple small lacunes (fig. le) were detected in the deep white mat­
ter on MRI. Quantitative rCBF measurement with SPECT brain
scan using 99raTc-HMPAO showed relative hypoperfusion localized
in the bilateral frontal lobes, with 46 and 47 m l/100 g/min in the right
and left frontal lobes, respectively, whereas the absolute values of
rCBF ranged from 50 to 59 nil/100 g/min in the other regions in the
cerebral cortex. Routine scalp EEG showed normal findings, consist­
ing of occipital-dominant background activities of 9-10 Hz mixed
with frontal-dominant fast activities o f20-25 Hz with no slow waves
or paroxysmal discharges. In recordings of event-related potentials,
P300 revealed relatively low amplitudes, with heights of 3.07 and
4.82 pV in Cz and Pz recordings, respectively, these latencies both
showing the normal value of 358 ms. Further, contingent negative
variations (CNVs) showed relatively low amplitudes with the heights
of the late CNV component in Fz and Cz recordings indicating 3.80
and 4.64 pV, respectively. In neuropsychologial tests, the WAIS-R
demonstrated average intelligence, with scores of 98. 87 and 93 for
verbal, performance and full IQ scores, respectively, although scores
on comprehension and combination tasks were relatively low. Fur­
ther, the Wechsler Memory Scale test demonstrated almost normal
memory function, which was however somewhat low as compared
with his intelligence level, with an MQ score of 90. In contrast, he
showed poor results on the Wisconsin Card Sorting test (WCST).
which is known as a test of basic abstract thinking and the ability to
shift simple mental sets [2], attaining only two categories (color and
figure) with frequent perseverative errors (13 in color and 57 in fig­
ure). In addition, laboratory examinations, including hematology,
liver function tests, electrolytes, urinalysis, ECG and blood pressure,
showed no abnormalities. Further, he showed no abnormalities in
otolaryngological examinations, including routine olfactory tests.
After these examinations, he was treated as an outpatient with a
representative antipsychotic, haloperidol 2.25 rng/day, as well as
biperiden 3 mg/day to prevent the haloperidol-induced extrapyramidal symptoms. The haloperidol exerted a slight but beneficial effect
on his delusions and the feeling of physical disorder in his tongue,
mouth and nose, because he appeared to be less nervous about them
after than before the administration. However, these symptoms per­
sisted even with a subsequent increase in the haloperidol dose. Pimo­
zide 3-6 mg/day was added but led to only slight improvement of
these symptoms.

ty is more likely to be due to atrophy rather than a devel­
opmental disorder in view of the patient’s advanced age
and MRI findings.
In conclusion, it is undetermined whether the illness in
the present case should be classified as organic delusional

syndrome or paranoid disorder on DSM-III-R. However,
in either case the present clear coexistence of the monosymptomatic delusion and organic frontal abnormality
implies that delusions are associated with frontal lobe
abnormality.

1 Benson DF, Stuss DT: Frontal lobe influences
on delusions: A clinical perspective. Schizophr
Bull 1990:16:403-411.
2 Goldberg TE, Weinberger DR, Berman KF,
Pliskin NH, Podd MH: Further evidence for
dementia of the prefrontal type in schizophre­
nia?: A controlled study of teaching the Wis­
consin Card Sorting Test. Arch Gen Psychiatry
1987;44:1008-1014.
3 Munro A: Monosymptomatic hypochondriacal
psychosis manifesting as delusions of parasito­
sis. Arch Dermatol 1978:114:940-943.

4 Miller BL, Lesser 1M: Late-life psychosis and
modem neuroimaging. Psychiatr Clin North
Am 1988:11:33-46.
5 Gustafson L: Frontal lobe degeneration of nonAlzheimer type. II. Clinical picture and differ­
ential diagnosis. Arch Gerontol Gcriatr 1987:6:
209-223.
6 Ncary D, Snowden JS, Northen B, Goulding P:
Dementia of frontal lobe type. J Neurol Neurosurg Psychiatry 1988;51:353-361.

7 Williamson P: Hypofrontality in schizophre­
nia: A review of the evidence. Can J Psychiatry
1987:32:399-404.
8 Andreasen N, Nasrallah HA, Dunn V, Olson
SC, Grove WM. Ehrhardt JC, Coffman JA,
Crossett JHW: Structural abnormalities in the
frontal system in schizophrenia. Arch Gen Psy­
chiatry 1986;43:136-144.
9 Young AH. Blackwood DHR. Roxborough H,
McQueen JK, Martin MJ, Kean D: A magnetic
resonance imaging study of schizophrenia:
Brain structure and clinical symptoms. Br. J
Psychiatry 1991:158:158-164.

10

Jibiki/Kagara/Kishizawa/Kurokawa/
Fukushima/Furuta/Y amaguchi

Delusion and Frontal Lobe

Downloaded by:
Karolinska Institutet, University Library
130.237.122.245 - 1/12/2019 1:43:31 AM

References